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      The inflammatory and metabolic status of patients with sudden-onset sensorineural hearing loss

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          Abstract

          Introduction

          Sudden sensorineural hearing loss (SSNHL) is a common emergency symptom in otolaryngology that requires immediate diagnosis and treatment. SSNHL has a multifactorial etiology, and its pathophysiologic mechanisms may be associated with inflammatory and metabolic changes that may affect the cochlear microenvironment or its nervous component, thus triggering the process or hindering hearing recovery. Therefore, the aim of this study was to assess metabolic and inflammatory changes to identify systemic parameters that could serve as prognostic factors for hearing recovery in patients with SSNHL.

          Materials and methods

          Thirty patients with a sudden hearing loss of at least 30 dB in three contiguous frequencies were enrolled in this study. Patients were followed up for 4 months and peripheral blood samples were collected at 7 days (V1), 30 days (V2) and 120 days (V3). Interleukins (IL)-1F7, IL-2, IL-4, IL-5, IL-6, IL-10, interferon γ (IFN-γ), tumor necrosis factor α (TNF-α) and adiponectin were quantified in serum. In addition, lipid and glycemic profiles as well as concentration of creatinine, uric acid, fructosamine, peroxide, total proteins and albumin were analyzed. Patients underwent weekly ear-specific hearing tests with standard pure tone thresholds for frequencies of 250–8,000 Hz, speech recognition threshold and word recognition score.

          Results

          Patients with SSNHL were divided into a group of patients who did not achieve hearing recovery ( n = 14) and another group who achieved complete and significant recovery ( n = 16). Most serologic parameters showed no significant changes or values indicating clinical changes. However, IFN-γ levels decreased by 36.3% between V1 and V2. The cytokine TNF-α showed a statistically significant decrease from V1 to V3 (from 22.91 to 10.34 pg./mL). Adiponectin showed a decrease from 553.7 ng/mL in V1 to 454.4 ng/mL in V3.

          Discussion

          Our results show that serologic cytokine levels change in the acute phase of manifestation of SSNHL and establish a parallel between systemic changes and improvements in hearing, especially TNF-α, which showed differences in hearing recovery. The use of IFN-γ, TNF-α and adiponectin may elucidate the clinical improvement in these patients.

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          Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge.

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            IL-6 in inflammation, immunity, and disease.

            Interleukin 6 (IL-6), promptly and transiently produced in response to infections and tissue injuries, contributes to host defense through the stimulation of acute phase responses, hematopoiesis, and immune reactions. Although its expression is strictly controlled by transcriptional and posttranscriptional mechanisms, dysregulated continual synthesis of IL-6 plays a pathological effect on chronic inflammation and autoimmunity. For this reason, tocilizumab, a humanized anti-IL-6 receptor antibody was developed. Various clinical trials have since shown the exceptional efficacy of tocilizumab, which resulted in its approval for the treatment of rheumatoid arthritis and juvenile idiopathic arthritis. Moreover, tocilizumab is expected to be effective for other intractable immune-mediated diseases. In this context, the mechanism for the continual synthesis of IL-6 needs to be elucidated to facilitate the development of more specific therapeutic approaches and analysis of the pathogenesis of specific diseases.
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              Control of adaptive immunity by the innate immune system.

              Microbial infections are recognized by the innate immune system both to elicit immediate defense and to generate long-lasting adaptive immunity. To detect and respond to vastly different groups of pathogens, the innate immune system uses several recognition systems that rely on sensing common structural and functional features associated with different classes of microorganisms. These recognition systems determine microbial location, viability, replication and pathogenicity. Detection of these features by recognition pathways of the innate immune system is translated into different classes of effector responses though specialized populations of dendritic cells. Multiple mechanisms for the induction of immune responses are variations on a common design principle wherein the cells that sense infections produce one set of cytokines to induce lymphocytes to produce another set of cytokines, which in turn activate effector responses. Here we discuss these emerging principles of innate control of adaptive immunity.
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                Author and article information

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                Journal
                Front Neurol
                Front Neurol
                Front. Neurol.
                Frontiers in Neurology
                Frontiers Media S.A.
                1664-2295
                02 July 2024
                2024
                : 15
                : 1382096
                Affiliations
                [1] 1ENT Research Lab, Department of Otorhinolaryngology—Head and Neck Surgery, Universidade Federal de São Paulo (UNIFESP) , São Paulo, Brazil
                [2] 2Post-Graduation Program in Health Sciences, Santo Amaro University (UNISA) , São Paulo, Brazil
                Author notes

                Edited by: Lisheng Yu, Peking University People’s Hospital, China

                Reviewed by: Sasa R. Vasilijic, Stanford University, United States

                Arwa Kurabi, University of California San Diego, United States

                *Correspondence: Jônatas Bussador do Amaral, jbamaral@ 123456unifesp.br
                Article
                10.3389/fneur.2024.1382096
                11250376
                39015324
                6caf6b76-b01a-4375-8009-73f7b055e6a5
                Copyright © 2024 do Amaral, Peron, Soeiro, Scott, Hortense, da Silva, França, Nali, Bachi and de Oliveira Penido.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 05 February 2024
                : 14 June 2024
                Page count
                Figures: 5, Tables: 3, Equations: 0, References: 85, Pages: 15, Words: 11710
                Funding
                The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. This work was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (Fapesp process number 2021/07346-6). Norma de Oliveira Penido received funding from National Council for Scientific and Technological Development (CNPq process number 302910/2020-4).
                Categories
                Neurology
                Original Research
                Custom metadata
                Neuro-Otology

                Neurology
                sudden sensorineural hearing loss,cytokines,inflammation,metabolism,adiponectin,ifnγ,tnf-α
                Neurology
                sudden sensorineural hearing loss, cytokines, inflammation, metabolism, adiponectin, ifnγ, tnf-α

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